In order to understand the mechanisms of HIV-1 infection kineticsin vivo, and how it affects pathogenesis and responses to antiretroviral treatment, we worked in several directions: 1) We completed our studies on therate of telomere length shortening as a measure of cell turnover - the major conclusion is that HIV infection modestly (2-3 fold) increases the turnover rateof T and B cells compared to uninfected humans and monkeys. We speculate that these results suggest an increase in the cell turnover rate due to the continuous activation of the immune system under the conditions of chronic exposure to antigen but not to exhaustion of the ability of the immune system toregenerate itself; 2) We analyzed the HIV infection kinetics under highly activeantiretroviral therapy and found that the HIV replication may not be completely inhibited; and 3) We continued to improve our method which allows long-term prediction of responses to antiretroviral treatment based on short-term measurements and derived a simple equation for long-term prognosis of drug efficacy. We also analyzed data for patients under highly active antiretroviral therapy where the therapy was stopped and restarted. The dynamics of cells labeled with BrdU or deutirated glucose measured in C. Lanes group are being analyzed. Z01 BC 10042-04 - chemotherapy, regulation, theoretical biology,